ライフサイエンスコーパス: pancreatic carcinoma

1 as 10 months and 13 months for patients with pancreatic carcinoma.

2 patients with suspected primary or recurrent pancreatic carcinoma.

3 useful in the chemoprevention and therapy of pancreatic carcinoma.

4 the rationale for molecular chemotherapy of pancreatic carcinoma.

5 of the Rb/p16 pathway in the development of pancreatic carcinoma.

6 ive pancreaticoduodenectomy in patients with pancreatic carcinoma.

7 cells that recognize CEA in a mouse model of pancreatic carcinoma.

8 as matched patients with conventional ductal pancreatic carcinoma.

9 or nuclear imaging and radioimmunotherapy of pancreatic carcinoma.

10 ful to differentiate focal inflammation from pancreatic carcinoma.

11 is and potential therapy of pancreatitis and pancreatic carcinoma.

12 s present in the setting of pancreatitis and pancreatic carcinoma.

13 --may also be an important mediator in human pancreatic carcinoma.

14 nt novel targets for aberrant methylation in pancreatic carcinoma.

15 ing healthy pancreas, from two patients with pancreatic carcinoma.

16 gemcitabine alone for patients with advanced pancreatic carcinoma.

17 ne that is inactivated in nearly half of all pancreatic carcinomas.

18 toplasmic COX-2 expression in 14 of 21 (67%) pancreatic carcinomas.

19 s examined by methylation-specific PCR in 18 pancreatic carcinomas.

20 than 50% incidence in colon and about 90% in pancreatic carcinomas.

21 6 gene was genetically inactivated in 82% of pancreatic carcinomas.

22 spontaneously develop autochthonous, lethal pancreatic carcinomas.

23 verlap in the mutational spectra of BDPs and pancreatic carcinomas.

24 ed in an independently analyzed series of 19 pancreatic carcinomas.

25 on or mutations of the gene were observed in pancreatic carcinomas.

26 quently in cell lines than in primary ductal pancreatic carcinomas.

27 1 involved by homozygous deletions in 30% of pancreatic carcinomas.

28 4 were inactivated in nearly one-half of the pancreatic carcinomas.

29 hydrolase that displays elevated activity in pancreatic carcinomas.

30 equently to the liver, consistent with human pancreatic carcinomas.

31 of pancreatic cancer cell lines and primary pancreatic carcinomas.

32 in pancreatic cancer cell lines and primary pancreatic carcinomas.

33 blinded serum samples from 26 patients with pancreatic carcinoma, 10 patients with chronic pancreati

34 mplification of AKT2 in approximately 10% of pancreatic carcinomas (2 of 18 cell lines and 1 of 10 pr

35 olled onto the study (gastric carcinoma, 31; pancreatic carcinoma, 22).

36 at whereas DPC4 inactivation is prevalent in pancreatic carcinoma (48%), it is distinctly uncommon (<

37 specificity than CT in correctly diagnosing pancreatic carcinoma (92% and 85% versus 65% and 61%).

38 specificity than CT in correctly diagnosing pancreatic carcinoma (92% and 85% vs. 65% and 62%).

39 tochemistry, we found that 57 of 61 invasive pancreatic carcinomas (93%), 3 of 18 high-grade pancreat

40 Pancreatic carcinoma affecting the uncinate process is a

41 Integrin alpha6beta4 is highly expressed in pancreatic carcinoma and contributes to cancer progressi

42 the presence of the same abnormal protein in pancreatic carcinoma and explore the molecular basis for

43 nology has been studied for the treatment of pancreatic carcinoma and has shown a significant surviva

44 ference suppresses PEG10 expression in Panc1 pancreatic carcinoma and HepG2 hepatocellular carcinoma

45 hat two human tumor cell lines, derived from pancreatic carcinoma and lung carcinoma, harbor homozygo

46 ammatory, and fibrogenic cellular subsets in pancreatic carcinoma and plays a central role in cross t

47 n of CPT-11 can decrease the growth of human pancreatic carcinoma and the incidence of metastasis in

48 ive pancreaticoduodenectomy in patients with pancreatic carcinoma and with local residual disease.

49 We studied 45 pancreatic carcinomas and 14 normal pancreata for aberra

50 cifically enhanced in blood vessels of human pancreatic carcinomas and in vessels of other tumor type

51 mutations are found in approximately 90% of pancreatic carcinomas and may contribute to the poor pro

52 suppressor is inactivated in nearly half of pancreatic carcinomas and to a lesser extent in a variet

53 obes on tumor tissues (cholangiocarcinoma or pancreatic carcinoma) and non-tumor tissues from 29 pati

54 or cell lines--U251 glioblastoma, MIA PaCa-2 pancreatic carcinoma, and the colon carcinomas SW620 and

55 ion of the preoperative diagnosis of primary pancreatic carcinoma, and the impact of 18FDG-PET on pat

56 of p16/CDKN2 were observed in three primary pancreatic carcinomas, and five primary tumors revealed

57 However, data for pancreatic carcinoma are limited.

58 was observed at 40 mg/kg in the BXPC3 human pancreatic carcinoma as well as in the H125 human non-sm

59 l cancers arising from colonic polyps, seven pancreatic carcinomas, as well as seven gastric cancers.

60 was seen selectively in colon, prostate, and pancreatic carcinomas but not in breast, lung, or ovaria

61 yglucose (FDG) PET scans in the diagnosis of pancreatic carcinoma by analyzing different cutoff level

62 conclusion, induction of MUC4 expression in pancreatic carcinoma by RA is mediated through the RAR-a

63 To date, 23 (64%) of 35 pancreatic carcinomas carry at least one homozygous dele

64 ine kinase inhibitor hindered HGF-stimulated pancreatic carcinoma cell chemotaxis and invasive growth

65 iated signaling pathway that regulates human pancreatic carcinoma cell invasion and metastasis, yet d

66 ha(v)beta(6) expression) or the BxPC-3 human pancreatic carcinoma cell line (endogenous alpha(v)beta(

67 tion was examined in a poorly differentiated pancreatic carcinoma cell line (Panc-1), possessing only

68 The changes mediated by VEGFR-1 in this pancreatic carcinoma cell line are highly consistent wit

69 ine HepG2, melanoma cell line SK-MEL-37, and pancreatic carcinoma cell line Capan-1 by the same mecha

70 Overexpression of KLF4 in a human pancreatic carcinoma cell line induced a significant dec

71 Treating the pancreatic carcinoma cell line MIA PaCa-2 with trichosta

72 TLs selectively lysed the p53-overexpressing pancreatic carcinoma cell line Panc-1 but did not recogn

73 In the pancreatic carcinoma cell line, BxPC3, the non-conservat

74 al level to induce p21(WAF1/CIP1) in a human pancreatic carcinoma cell line, Panc-1.

75 n in apoptosis induction in the BxPC-3 human pancreatic carcinoma cell line.

76 d by the Western blot assay in three of five pancreatic carcinoma cell lines (BxPC-3, Capan-1, and MD

77 We find that MLL2 is amplified in two of 14 pancreatic carcinoma cell lines and one of five glioblas

78 he potential bystander effect in established pancreatic carcinoma cell lines and patient-derived tumo

79 pliced variant form of PAX6, is expressed in pancreatic carcinoma cell lines at higher levels than th

80 However, four of five pancreatic carcinoma cell lines exhibited either elevate

81 tion, which demonstrated that 18 of 19 (95%) pancreatic carcinoma cell lines expressed S100A4.

82 We show that two pancreatic carcinoma cell lines known to have either wil

83 on of MEK1 in a number of human melanoma and pancreatic carcinoma cell lines led to reduced cell surf

84 We found that human pancreatic carcinoma cell lines that have undergone dele

85 l resection of their carcinomas and 18 human pancreatic carcinoma cell lines were analyzed by single-

86 Five of the eight pancreatic carcinoma cell lines were p16(-), MTAP was co

87 odel systems, the MiaPaCa-2 and PANC-1 human pancreatic carcinoma cell lines, by transfection with MT

88 Here we show that in two pancreatic carcinoma cell lines, PT45 and Panc-1, that a

89 epatocellular, salivary gland, cervical, and pancreatic carcinoma cell lines.

90 ows the importance of the uPA/uPAR system in pancreatic carcinoma cell migration and invasion.

91 loading of Rap1 is specifically required for pancreatic carcinoma cell migration on vitronectin but n

92 cetylase inhibitors (HDACI) interact to kill pancreatic carcinoma cells and determined the impact of

93 sively in highly invasive colon, breast, and pancreatic carcinoma cells and not in their poorly invas

94 al PKC/PKD signaling pathway in human ductal pancreatic carcinoma cells and suggest that PKCs mediate

95 e were injected intraperitoneally with human pancreatic carcinoma cells and treated with GCV (50 mg/k

96 Pancreatic carcinoma cells are highly susceptible to tra

97 ently ubiquitous antitumor effects of mda-7, pancreatic carcinoma cells are remarkably refractory to

98 ondrial dysfunction in MIA PaCa-2 and PANC-1 pancreatic carcinoma cells both detached and attached to

99 ) can inhibit growth and metastasis of human pancreatic carcinoma cells implanted into the pancreas o

100 Calu-1 and A-549 lung carcinoma and Colo 357 pancreatic carcinoma cells in G2/M, T-24 bladder carcino

101 t CEA can eradicate tumors grown from CEA(+) pancreatic carcinoma cells in the pancreas of CEAtg mice

102 arget by showing that activation of RIG-I in pancreatic carcinoma cells induced IRF-3 phosphorylation

103 Analysis of signal transduction changes in pancreatic carcinoma cells infected with Ad.mda-7 in com

104 neered resistance to mda-7/IL-24, as well as pancreatic carcinoma cells inherently resistant to any t

105 fonic acid), against highly metastatic human pancreatic carcinoma cells injected into the pancreas of

106 In this study, we isografted PanO2 pancreatic carcinoma cells into mice in which LRP1 was d

107 epidermal growth factor (EGF) stimulation of pancreatic carcinoma cells led to invasion and metastasi

108 Pancreatic carcinoma cells lines are known to have a hig

109 GF)-mediated migration and invasion of human pancreatic carcinoma cells require uPA and uPAR function

110 sis, PANC1 cells and ASPC1 cells, as well as pancreatic carcinoma cells that do not overexpress AKT2

111 Moreover, transfection of mutant K-ras pancreatic carcinoma cells with an antisense K-ras expre

112 he in vitro motility and invasiveness of the pancreatic carcinoma cells without affecting their growt

113 In mutant K-ras pancreatic carcinoma cells, programmed cell death correl

114 en together, our results show that in AsPC-1 pancreatic carcinoma cells, Sp1-dependent VPF/VEGF trans

115 ediated tumor cell invasion and migration in pancreatic carcinoma cells, we hypothesize that VEGFR-1

116 effects of TGFbeta in human osteosarcoma and pancreatic carcinoma cells.

117 ine-like phenotype) in poorly-differentiated pancreatic carcinoma cells.

118 inoma cells, and BxPC-3 and MDAPanc-28 human pancreatic carcinoma cells.

119 s on the growth and survival of K-ras mutant pancreatic carcinoma cells.

120 lfoam saturated with conditioned medium from pancreatic carcinoma cells.

121 21%, and 4% phosphorylation in PANC-1 (human pancreatic carcinoma), CFPAC-1 (human metastatic ductal

122 he median survival of patients with advanced pancreatic carcinoma compared with single-agent gemcitab

123 Increased expression of Mirk was seen in pancreatic carcinomas compared with primary cultures of

124 K-3beta) is overexpressed in human colon and pancreatic carcinomas, contributing to cancer cell proli

125 olon carcinoma CX-1, breast carcinoma MCF-7, pancreatic carcinoma (CRL 1420, bladder transitional cel

126 Ductal pancreatic carcinoma (DPC) is a deadly disease with an i

127 the invasive/metastatic properties of human pancreatic carcinomas driven by EGFR.

128 that ST6Gal-I is upregulated in ovarian and pancreatic carcinomas, enriched in metastatic tumors, an

129 Pancreatic carcinomas express high levels of urokinase-t

130 Because most pancreatic carcinomas express S100A4, it may be a useful

131 Here, we analyzed pancreatic carcinomas for additional mechanisms by which

132 To screen pancreatic carcinomas for chromosomal aberrations we hav

133 Pancreatic carcinomas from cigarette smokers harbor more

134 Thirty microdissected primary human ductal pancreatic carcinomas from patients not subject to radio

135 rg(-/-) mice challenged with fibrosarcoma or pancreatic carcinoma grow larger tumors with increased m

136 a pancreatic carcinoma; indeed, an excess of pancreatic carcinoma has been seen in some BRCA2 cancer

137 th pancreaticoduodenectomy for patients with pancreatic carcinoma have clearly established a role for

138 glioblastomas, CALU-6 lung carcinoma, ASPC-1 pancreatic carcinoma, HT-29 and HCT-116 colon carcinomas

139 Thus, we conclude that many pancreatic carcinomas hypermethylate a small percentage

140 vated K-Ras can promote radiation killing of pancreatic carcinoma in a superadditive manner.

141 d, hence, the growth and metastasis of human pancreatic carcinoma in nude mice.

142 Of the 32,180 patients diagnosed with pancreatic carcinoma in the United States this year, app

143 al invasion, and hepatic metastasis of human pancreatic carcinomas in mice.

144 Finally, for pancreatic carcinoma, in which local control is an even

145 ne was aided by its homozygous deletion in a pancreatic carcinoma; indeed, an excess of pancreatic ca

146 les of the juxtatumoral stroma in breast and pancreatic carcinomas indicated important differences be

147 gene (a gene that is mutated in 85 to 95% of pancreatic carcinomas), induces a dramatic suppression i

148 Pancreatic carcinoma is a malignant disease that respond

149 r the diagnosis and distinguishing them from pancreatic carcinoma, is detection of fatty tissue on CT

150 Highly metastatic human pancreatic carcinoma L3.6pl cells were injected into the

151 n metastasis, was expressed in five of seven pancreatic carcinoma libraries but not in the two normal

152 mor cell line, TMPRSS2 on 21q in the Bx PC-3 pancreatic carcinoma line, and Cadherin 6 (CDH6) on 5p i

153 MTAP(+) normal keratinocytes and pancreatic carcinoma lines had relatively poor sensitivi

154 Seven human pancreatic carcinoma lines with activated K-ras and two

155 Smad4, also known as deleted in pancreatic carcinoma locus 4 (DPC4), is a critical co-fa

156 Deletion of SMAD4/DPC4 (deleted in pancreatic carcinoma locus 4) occurs in approximately 50

157 e association with the product of deleted in pancreatic carcinoma, locus 4 (DPC4), Smad4.

158 Specifically, DPC4 (deleted in pancreatic carcinoma, locus 4 or MADH4/SMAD4) is a tumor

159 Therefore, the containment of pancreatic carcinoma makes it amenable to this gene ther

160 tric genes had previously been considered as pancreatic carcinoma markers.

161 man prostate adenocarcinoma DU-145 and human pancreatic carcinoma MiaPaCa-2 cells as a model, we now

162 Suppression of this activity in pancreatic carcinoma might, therefore, facilitate tumor

163 These signaling events, in turn, promote pancreatic carcinoma migration and invasion.

164 ndent of initial tumor volume (in the ASPC-1 pancreatic carcinoma model) and reversible on withdrawal

165 melanoma model and the Rip-Tag2 spontaneous pancreatic carcinoma model.

166 4 correlated with Apo2L/TRAIL sensitivity in pancreatic carcinoma, non-small-cell lung carcinoma and

167 In vitro studies using human pancreatic carcinoma PANC-1 cells proved that these PSiN

168 receptor 4 (FGFR4) is expressed in 50-70% of pancreatic carcinomas (PC) and a similar proportion of d

169 In addition, in a panel of 45 pancreatic carcinomas prescreened for loss of heterozygo

170 could therefore be of use as sensitizers for pancreatic carcinoma radiotherapy.

171 ure of invasion sites in human prostatic and pancreatic carcinoma samples.

172 Chronic pancreatitis and pancreatic carcinoma show abnormal pancreatic enhancemen

173 About 90 percent of human pancreatic carcinomas show allelic loss at chromosome 18

174 4, FBW7, AGO, SEL10) related to two distinct pancreatic carcinoma subsets: the medullary KRAS2-wild-t

175 have been previously described in classical pancreatic carcinomas such as lipocalin 2, galectin 3, c

176 tial fraction of breast, prostate, lung, and pancreatic carcinomas, suggesting a potential tumor supp

177 e differentially expressed both in IPMTs and pancreatic carcinomas suggests that they may be involved

178 d in similar grade PanINs from patients with pancreatic carcinoma than in those with other pancreatic

179 PSCA is a novel tumor marker for pancreatic carcinoma that has potential diagnostic and t

180 ally, a Smad4 mutation identified in a human pancreatic carcinoma that inactivates Smad4 signaling ab

181 tations in DPC4 were identified in six of 27 pancreatic carcinomas that did not have homozygous delet

182 Among the 21 assessable patients with pancreatic carcinoma, there was one responder.

183 In pancreatic carcinomas, this tumor suppressive activity i

184 rcinoma, T241 fibrosarcoma) and human (BxPC3 pancreatic carcinoma) tumors.

185 These data suggest that the majority of pancreatic carcinomas undergo selection for hypomethylat

186 y-five patients who presented with suspected pancreatic carcinoma underwent whole-body FDG PET in add

187 For some solid tumors, such as pancreatic carcinoma, using a time-to-event end point (e

188 In a genetic model of pancreatic carcinoma, vaccination with ENO1 DNA elicits

189 of the PanINs from the 14 pancreata without pancreatic carcinoma was unmethylated with respect to ei

190 Here, using an orthotopic mouse model of pancreatic carcinoma, we evaluated L1 functionality in c

191 In an orthotopic mouse model of human pancreatic carcinoma, we evaluated the effect of anti-uP

192 To determine the involvement of BRCA2 in pancreatic carcinomas, we screened for BRCA2 alterations

193 te tumor suppressor genes on 18q, a panel of pancreatic carcinomas were analyzed for convergent sites

194 to be up-regulated in prostate, breast, and pancreatic carcinomas were discovered by DDD, demonstrat

195 Fifty-two patients had proven pancreatic carcinoma, whereas 13 had benign lesions, inc

196 r 2) previously shown to be overexpressed in pancreatic carcinoma, whereas the third tag corresponded

197 hows that TLR9 has protumorigenic effects in pancreatic carcinoma which are distinct from its influen

198 tide group (three cardiovascular deaths, one pancreatic carcinoma, which was assessed as being possib

199 easing knowledge of the molecular biology of pancreatic carcinoma will lead to improvements in diagno

200 ngle center's experience in the treatment of pancreatic carcinoma with a combination of pancreatic re

201 ients undergoing pancreaticoduodenectomy for pancreatic carcinoma with gross or microscopic evidence

202 cing and in two cell lines and three primary pancreatic carcinomas with a reduced or absent expressio

203 We identify pancreatic carcinomas with BRAF deletions mutually exclu

204 omas in a previously characterized series of pancreatic carcinomas with known K-ras mutational status

205 ant antineoplastic activity in MUC1-positive pancreatic carcinoma xenografts as compared to mock inoc